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- W2071388976 abstract "Norepinephrine release from spinal synaptosomes. (Wake Forest University School of Medicine, Winston‐Salem, NC) Anesthesiology 2000;93:164–172. The purpose of this study was to determine if clonidine could inhibit release of NE in a preparation of spinal cord tissue lacking synaptic circuits. Crude synaptosomes were prepared from male Sprague‐Dawley rat spinal cord, loaded with [ 3 H]NE, and stimulated by potassium chloride to release [ 3 H]NE. Samples were incubated with clonidine in the absence or presence of various inhibitors. To study the effect of α 2A ‐adrenergic receptor subtypes, some animals were pretreated with an oligodeoxynucleotide (ODN) composed of a sense or antisense sequence to a portion of this receptor. Potassium chloride produced a concentration‐dependent increase in [ 3 H]NE release, and this release was inhibited by clonidine with a concentration producing 50% maximal inhibition (IC 50 ) of 1.3 μ m . The effect of clonidine was inhibited by the α 2A ‐adrenergic antagonists, yohimbine, and idazoxan, but not by α 1A ‐adrenergic, muscarinic, or opioid antagonists. Intrathecal pretreatment with antisense ODN to α 2A ‐adrenergic receptors reduced α 2A ‐adrenergic receptor protein expression compared with sense ODN control and also reduced clonidine‐induced inhibition of [ 3 H]NE release. Conclude that these data demonstrate the existence of classic autoinhibitory α 2A ‐adrenergic receptors in the spinal cord, probably of the α 2A subtype. They further suggest that clonidine‐induced stimulation of spinal NE release must occur from indirect actions, presumably due to activation of a spinal circuit." @default.
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- W2071388976 date "2001-01-01" @default.
- W2071388976 modified "2023-10-16" @default.
- W2071388976 title "Basic Science (24)" @default.
- W2071388976 doi "https://doi.org/10.1111/j.1533-2500.2001.1011-24.x" @default.
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